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Zinc oxide nanostructures such as nanosheets (NS) and nanoflowers (NF) were obtained by a facile hydrothermal synthesis using zinc chloride (ZnCl2) as precursor with low molar concentrations and a short synthesis time (2 h) at 200 °C. By means of X-ray diffraction and Raman spectroscopy measurements, the wurtzite-type ZnO structure was confirmed with high crystalline quality. SEM micrographs showed the influence of ZnCl2 concentration on ZnO morphology; ZnO NF were obtained at low concentrations (0.02 and 0.05 M), while ZnO NS were seen for higher concentrations (0.2-0.6 M) and their thicknesses can be estimated from 15 to 60 nm. In addition, TEM images showed a large number of pores with sizes below 15 nm in both ZnO nanostructures. Raman and photoluminescence displayed the surface defects density for ZnO nanostructures. Raman spectra showed the E1(LO) mode localized at ∼581 cm-1, associated with oxygen vacancies and zinc interstitials, being more intense for ZnO NF, while photoluminescence results showed a strong yellow-orange emission (centered from 587 to 618 nm) relative to UV emission, being more intense for ZnO NF. These properties reveal further potential for high performance luminescent devices based on ZnO NF and NS.

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INTRODUCTION: Germ cell tumours (GCTs) of the testis show exquisite sensitivity to treatment with cisplatin. Despite the high cure rates provided by platinum-based chemotherapy, 10-20% of patients die from progressive disease. Although various cellular pathways may influence cisplatin efficacy, their actual impact has not been comprehensively investigated in advanced GCTs. The objective of the present study was to clarify the role of the expression status of proteins involved in the Rb and p53 tumour suppressor pathways in sensitivity and resistance of GCTs to cisplatin-based chemotherapy. MATERIALS AND METHODS: Paraffin-embedded tumour tissues from 84 patients with advanced GCT treated with cisplatin-based chemotherapy were analysed. Immunohistochemical expression of proteins p53 and mdm2, and the G1-phase cyclins D1 and D2 (CD1 and CD2) was assessed and correlated with the clinical course. RESULTS: The percentages of positive expression of p53, mdm2, CD1 and CD2 were 56, 57, 37.5 and 55%, respectively. From univariate analysis, there was no significant association between p53, mdm2 or CD1 expression and outcome. Instead, positive CD2 expression was found to be marginally associated with shorter median duration of progression-free survival (PFS) (p=0.06). In multivariate analysis, none of the molecular markers retained statistical significance with treatment response or survival. CONCLUSIONS: Tissular expression of p53, mdm2 and CD1 is not associated with prognosis or treatment response in patients with advanced GCT. Aberrant CD2 expression appears to further determine a shorter PFS. Larger and further studies are required to validate CD2 as a marker of cisplatin resistance (AU)

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BACKGROUND: Germ cell tumours (GCTs) represent an extraordinarily chemosensitive malignancy. However, 20-30% of patients with advanced disease cannot be cured by currently available treatments. The role of tyrosine kinase receptors has been widely studied in other malignancies. Yet, limited information is available on GCTs. METHODS: One hundred and nine paraffin-embedded GCTs in 84 patients were assessed by immunohistochemistry for epidermal growth factor receptor (EGFR), human epidermal growth factor receptor 2 (HER-2)/neu and KIT (CD117) expression. Univariate and multivariate analyses were performed to evaluate their role as predictive and/or prognostic factors. RESULTS: EGFR and HER-2/neu staining was detected in 28% and 13% of tumours, respectively, predominantly in nonseminomatous GCTs. KIT protein was almost universally expressed in seminomas (97%), being virtually absent in choriocarcinoma and teratocarcinoma subtypes. EGFR expression showed inverse association with tumour response of borderline significance. With a median follow-up of 10.6 years, no significant association was observed between the expression of any of these markers and relapse-free or overall survival. CONCLUSIONS: EGFR, HER-2/neu and KIT have differential patterns of expression in GCTs according to histological subtypes. The expression of these markers in our series had no prognostic or predictive significance (AU)

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OBJECTIVE: The role of molecular and biological factors in ovarian cancer is controversial. We investigated the levels of the estrogen (ER) and progesterone (PR) receptors, HER2/neu, p-53 and Ki 67 in patients with advanced ovarian cancer and correlated the results with the clinical course in order to define their predictive or prognostic significance. METHODS: Paraffin-embedded tumor tissues from 72 patients with ovarian cancer treated from 1999 to 2003 were analyzed. Overexpression of C-erb-B2 was defined as herceptest ++/+++ and positive fluorescence in situ hybridization (FISH) or herceptest +++/+++. Positivity for ER and PR was determined by > or =10% of the cellular membranes immunostained. Statistical analysis was performed to evaluate the prognostic impact of the molecular markers. RESULTS: 49 of the 72 patients were ER + (68%) and 36 PR + (50%). In 45 patients (62.5%) expression of p53 was > or =10%. Overexpression of C-erb-2 was found in 4 tumor samples (5%). A Ki67 labelled nuclear area >30% was found to be associated with a higher rate of complete response (chi(2); p=0.05). None of the biological markers were significantly associated with progression free survival (PFS). By multivariate analysis residual tumor after debulking surgery and ER status were associated with OS (p< or =0.05). CONCLUSIONS: Ki67 nuclear expression >30% is predictive of complete response in advanced ovarian cancer. HER2/neu overexpression is scarce in our study. Positive ER is an independent prognostic factor for OS. Further research with larger studies and hormonal treatment is guaranteed.

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OBJECTIVE: The role of molecular and biological factors in ovarian cancer is controversial. We investigated the levels of the estrogen (ER) and progesterone (PR) receptors, HER2/neu, p-53 and Ki 67 in patients with advanced ovarian cancer and correlated the results with the clinical course in order to define their predictive or prognostic significance. METHODS: Paraffin-embedded tumor tissues from 72 patients with ovarian cancer treated from 1999 to 2003 were analyzed. Overexpression of C-erb-B2 was defined as herceptest ++/+++ and positive fluorescence in situ hybridization (FISH) or herceptest +++/+++. Positivity for ER and PR was determined by > or =10% of the cellular membranes immunostained. Statistical analysis was performed to evaluate the prognostic impact of the molecular markers. RESULTS: 49 of the 72 patients were ER + (68%) and 36 PR + (50%). In 45 patients (62.5%) expression of p53 was > or =10%. Overexpression of C-erb-2 was found in 4 tumor samples (5%). A Ki67 labelled nuclear area >30% was found to be associated with a higher rate of complete response (chi(2); p=0.05). None of the biological markers were significantly associated with progression free survival (PFS). By multivariate analysis residual tumor after debulking surgery and ER status were associated with OS (p< or =0.05). CONCLUSIONS: Ki67 nuclear expression >30% is predictive of complete response in advanced ovarian cancer. HER2/neu overexpression is scarce in our study. Positive ER is an independent prognostic factor for OS. Further research with larger studies and hormonal treatment is guaranteed (AU)

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- Propósito: Descripción del patrón característico de disemimación metastática peritoneal del carcinoma lobulillar infiltrante de mama.- Material y métodos: Describimos tres casos de carcinomatosis peritoneal secundaria a la diseminación metastática de carcinoma lobulillar infiltrante de mama. Dos de nuestras pacientes fueron diagnosticadas de carcinomatosis peritoneal como primera manifestación de un carcinoma lobulillar de mama, y la tercera diesiciete años después de su diagnóstico inicial. - Discusión: Las metástasis peritoneales en una paciente con un carcinoma de mama son poco frecuente, pero cuando aparecen suelen ser secundarias a un carcinoma lobulillar infiltrante de mama con receptores hormonales positivos. La inespecificidad de los síntomas junto a un intervalo normalmente largo, incluso de años después de un diagnóstico inicial del tumor, hace difícil diferenciar desde el punto de vista clínico entre un tumor primario de la cavidad peritoneal o la presencia de metástasis de un carcinoma de mama. Este diagnóstico se vuelve aún más complicado cuando la lesión metastática peritoneal es la primera manifestación del cáncer de mama, como ocurrió en dos de nuestras pacientes. Los estudios de inmunohistoquímica pueden ser útiles para lograr un diagnóstico correcto. Los marcadores más informativos son la proteína 15 del flujo de los quistes mamarios (GCDFP-15:gross cystic disease fluid protein-15), y los receptores de estrógeno y progesterona. La identificación de esta entidad es importante para el oncólogo, condiciona el pronóstico y la elección de modalidades terapéuticas adecuadas que difieren a la de otros tumores que también pueden cursar con carcinomatosis peritoneal en su evolución. La quimioterapia y sobre todo la hormonoterapia, tanto los antiestrógenos como los inhibidores de la enzima aromatasa, en tumores con receptores hormonales positivos, puede ser efectiva con remisiones parciales o completas del tumor, que en algunos casos son prolongadas en el tiempo (AU)

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The syndrome of mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS) is a multisystemic disorder associated in most of the patients with an A to G transition at nucleotide position 3243 in the transfer RNA (tRNA)Leu(UUR) (A3243G) of the mitochondrial DNA. This syndrome is characterized by the preponderant involvement of skeletal muscle and central nervous system, but urinary or gastrointestinal symptoms are seldom documented. Here we report an unusual case of a 52-year-old woman with a clinical phenotype characterized by encephalopathy, left hemiparesis, urinary retention and gastrointestinal pseudo-obstruction. She had the classical A3243G mitochondrial DNA point mutation of MELAS syndrome. We also present a clinically heterogeneous multigenerational pedigree with several affected members in the maternal lineage.

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